ArticleCureus2026
Case Report of Initial Manifestation of Hypogonadotropic Hypogonadism Based on Unoccluded Growth Plates in a 26-Year-Old Vietnamese Patient.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Hypogonadotropic hypogonadism is a rare endocrine disorder characterized by deficient secretion of gonadotropin-releasing hormone (GnRH), leading to reduced levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), ultimately resulting in impaired sexual maturation and pubertal development. While typically diagnosed during adolescence, rare cases present in adulthood as incidental findings. This case report describes an unusual presentation of hypogonadotropic hypogonadism discovered incidentally during treatment of a traumatic tibial fracture in a 26-year-old male patient, highlighting the importance of recognizing unoccluded growth plates as a potential indicator of underlying endocrine pathology. A 26-year-old Vietnamese male (height 1.70 m, weight 59 kg, BMI 20.4 kg/m²) presented to the emergency department on December 27, 2022, with left lower leg pain following a work-related accident. Radiographic imaging revealed a spiral fracture of the left tibial shaft with notably unoccluded growth plates. Physical examination demonstrated absent secondary sexual characteristics, including lack of pubic hair and prepubertal genitalia. The patient reported no previous medical conditions or current medications, though his history included mumps at age 10, raising the possibility of orchitis. Serial laboratory measurements over three consecutive days (at 8:45 AM each day) revealed consistently low serum testosterone (15.0-20.0 ng/dL; reference: 249-836 ng/dL), LH (0.17-0.22 IU/L; reference: 1.70-8.60 IU/L), and FSH (0.66-0.69 IU/L; reference: 1.50-12.4 IU/L), confirming the diagnosis of hypogonadotropic hypogonadism. Other pituitary function tests were within normal limits. The tibial fracture was treated with closed reduction and intramedullary interlocking nail fixation. Following endocrinological consultation, the patient was initiated on testosterone replacement therapy administered every three months. This case demonstrates an uncommon adult presentation of hypogonadotropic hypogonadism diagnosed incidentally following traumatic injury. The presence of unoccluded growth plates on routine radiographic imaging in an adult patient served as a crucial diagnostic clue, emphasizing the importance of systematic evaluation of skeletal maturity and endocrine status when such findings are encountered. Early recognition and appropriate hormonal replacement therapy are essential for addressing both the endocrine deficiency and potential skeletal complications. Long-term follow-up will determine the effectiveness of testosterone therapy and whether growth plate closure can be achieved.
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